Erythrocyte aggregation in patients with systemic lupus erythematosus

Spengler, M.; Svetaz, María J.; Leroux, María Bibiana; Bertoluzzo, S. M.; Carrara, Paolo; Isseldyk, F Van; Petrelli, D; Parente, F M; Bosch, Pau

doi:10.3233/ch-2011-1409

Cited by 24 publications

(13 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A growing interest has been recently devoted to the study of RBC aggregation and its impact on hemodynamics [5]. In addition, several studies reported association between RBC aggregation abnormalities and diseases, probably as a consequence of inflammation and/or metabolic disturbances, such as in primary open-angle glaucoma [56], type 2 diabetes [75], insulin resistance [15,16], sickle cell disease [49,83,93] and others [32,48,58,79,95]. Few studies have investigated RBC aggregation in response to exercise and contrasting results have been reported: some studies described no change [25,84,89], an increase, in association or not with a rise in plasma fibrinogen level [18,36,84], or a delayed decrease [98] with exercise.…”

Section: Red Blood Cell Aggregationmentioning

confidence: 99%

Exercise hemorheology: Classical data, recent findings and unresolved issues

Connes

Simmonds

Brun

et al. 2013

Clinical Hemorheology and Microcirculation

125

View full text Add to dashboard Cite

The present review focuses on the past and recent knowledge in the field of exercise hemorheology and presents some unresolved issues for opening discussion. Acute exercise is associated with a rise in hematocrit which results in an increase in blood viscosity. Whereas increased blood viscosity was previously viewed as having negative consequences for cardiovascular function and aerobic performance, recent findings suggest dynamic changes in blood viscosity might be useful for vascular function during exercise by increasing nitric oxide production. Other determinants of blood viscosity are altered by exercise (e.g., decreased red blood cell deformability, increased red blood cell aggregation and plasma viscosity) and may, independent of the associated effect on blood viscosity, directly modulate aerobic capacity. However, the data published on the effects of exercise on the hemorheology are not consistent, with some studies showing decreased, unchanged, or increased red blood cell deformability/aggregation when compared with rest. These discrepancies seem to be related to the exercise protocol investigated, the population tested or the methodogy utilized for hemorheological measurements. Finally, this review focuses on the effects of exercise training (i.e. chronic physical activity) on the hemorheological profile of healthy individuals and patients with cardiovascular and metabolic disorders. P. Connes et al. / Blood rheology and exerciseaddress classical findings in exercise hemorheology and will present new directions. In addition, some unresolved issues will be presented for opening discussion. Acute effects of exercise on hemorheology and relationships with performance2.1. Blood viscosity P. Connes et al. / Blood rheology and exercise 189 PRE 90 Blood viscosity (mPa/s) POST 90 POST 225 5 6 7 8 9

show abstract

Section: Red Blood Cell Aggregationmentioning

confidence: 99%

Exercise hemorheology: Classical data, recent findings and unresolved issues

Connes

Simmonds

Brun

et al. 2013

Clinical Hemorheology and Microcirculation

125

View full text Add to dashboard Cite

show abstract

“…Chronic inflammatory disorders are usually associated with high RBC aggregation; rheumatoid arthritis is a classic example of enhanced RBC aggregation due to chronic inflammation. Other autoimmune, inflammatory diseases such as systemic lupus erytematosus (SLE) have been reported to manifest high RBC aggregation [118,126]; Spengler, et al reported positive correlations of RBC aggregation with fibrinogen and with immunoglobulins in patients with SLE [118].…”

Section: Hematological Diseasesmentioning

confidence: 99%

Erythrocyte aggregation: Basic aspects and clinical importance

Başkurt

Meiselman

2013

Clinical Hemorheology and Microcirculation

171

130

View full text Add to dashboard Cite

Red blood cells (RBC) aggregate to form two-and three-dimensional structures when suspended in aqueous solutions containing large plasma proteins or polymers; this aggregation is reversible and shear dependent (i.e., dispersed at high shear and reformed at low or stasis). The extent of aggregation is the main determinant of low shear blood viscosity, thus predicting an inverse relationship between aggregation and in vivo blood flow. However, the effects of aggregation on hemodynamic mechanisms (e.g., plasma skimming, Fåhraeus Effect, microvascular hematocrit) may promote rather than impede vascular blood flow. The impact of enhanced RBC aggregation on endothelial function and hemostatic mechanisms adds further complexity, thereby requiring specific attention to the nature, extent and time course of aggregation when considering its overall influence on tissue perfusion. A detailed understanding of aggregation effects is important from a clinical point of view since it may be enhanced during a variety of pathophysiological processes, including infections, circulatory and metabolic disorders, hematological pathologies and several other disease states. Altered RBC aggregation may be an indicator of disease as well as a factor affecting the course of the clinical condition; the prognostic value of RBC aggregation indices has been demonstrated in various diseases. Currently, RBC aggregation is an easily and accurately measurable parameter, and therefore may be expected to have broader clinical usage in the future.

show abstract

“…This review will briefly summarize what is currently known about the involvement of RBCs in hemostasis and thrombosis and its underappreciated importance. RBCs increase blood viscosity because of a rise in hematocrit, an increase in RBC aggregation or a decrease in RBC deformability (increasing flow resistance) Pro [2][3][4][5] Conversely, anemia is associated with low blood viscosity and bleeding tendency as a result of reduced platelet margination toward endothelium and enhanced NO availability Anti [2][3][4][5] RBCs undergo shear-dependent reversible aggregation mediated by plasma proteins (mainly fibrinogen and immunoglobulins) and/or local osmotic gradient Pro [14][15][16][70][71][72][73][74] RBCs with increased rigidity occlude small vessels Pro [11,12] Deformability of RBCs reduces frictional resistance to flow Anti [8,[11][12][13]] RBCs maintain biconcave shape and a high surface-to-volume ratio as a result of cytoskeleton and water/ions balance Pro or anti [5] RBCs migrate to the center of blood flow and push platelets toward the endothelium (margination) in a hematocrit-and shear-dependent manner Pro [59][60][61] Effects on platelet reactivity RBCs increase platelet adhesion and aggregation by release of ADP and thromboxane A 2 Pro [66,67] RBCs form aggregates with platelets via adhesive molecules (ICAM-4 and fibrinogen with aIIbb3)…”

Section: Introductionmentioning

confidence: 99%

Red blood cells: the forgotten player in hemostasis and thrombosis

Weisel

Litvinov

2019

Journal of Thrombosis and Haemostasis

327

272

View full text Add to dashboard Cite

Summary New evidence has stirred up a long‐standing but undeservedly forgotten interest in the role of erythrocytes, or red blood cells (RBCs), in blood clotting and its disorders. This review summarizes the most recent research that describes the involvement of RBCs in hemostasis and thrombosis. There are both quantitative and qualitative changes in RBCs that affect bleeding and thrombosis, as well as interactions of RBCs with cellular and molecular components of the hemostatic system. The changes in RBCs that affect hemostasis and thrombosis include RBC counts or hematocrit (modulating blood rheology through viscosity) and qualitative changes, such as deformability, aggregation, expression of adhesive proteins and phosphatidylserine, release of extracellular microvesicles, and hemolysis. The pathogenic mechanisms implicated in thrombotic and hemorrhagic risk include variable adherence of RBCs to the vessel wall, which depends on the functional state of RBCs and/or endothelium, modulation of platelet reactivity and platelet margination, alterations of fibrin structure and reduced susceptibility to fibrinolysis, modulation of nitric oxide availability, and the levels of von Willebrand factor and factor VIII in blood related to the ABO blood group system. RBCs are involved in platelet‐driven contraction of clots and thrombi that results in formation of a tightly packed array of polyhedral erythrocytes, or polyhedrocytes, which comprises a nearly impermeable barrier that is important for hemostasis and wound healing. The revisited notion of the importance of RBCs is largely based on clinical and experimental associations between RBCs and thrombosis or bleeding, implying that RBCs are a prospective therapeutic target in hemostatic and thrombotic disorders.

show abstract

Erythrocyte aggregation in patients with systemic lupus erythematosus

Cited by 24 publications

References 31 publications

Exercise hemorheology: Classical data, recent findings and unresolved issues

Exercise hemorheology: Classical data, recent findings and unresolved issues

Erythrocyte aggregation: Basic aspects and clinical importance

Red blood cells: the forgotten player in hemostasis and thrombosis

Contact Info

Product

Resources

About